Minor physical anomalies in familial and sporadic schizophrenia: the Maudsley family study
a Wellcome Department
of Cognitive Neurology, Institute of Neurology, 12 Queen Square,
London, WC1N 3BG,UK, b Department of
Clinical Neuroscience, Newcastle University Medical School, Newcastle
upon Tyne, NE2 4HH, UK, c Department of
Psychological Medicine, Institute of Psychiatry, De Crespigny Park,
Denmark Hill, London, SE5 8AF, UK
Correspondence to: Dr T D Griffiths, Department of Physiological Sciences, Newcastle University Medical School, Newcastle upon Tyne, NE2 4HH, UK.
Received 16 October 1996 and in revised form 14 July 1997;
Accepted 17 July 1997
OBJECTIVES
(1) To test the hypothesis that minor
physical anomalies are increased in patients with schizophrenia and (2)
to investigate differences in the prevalence of minor physical
anomalies in patients with familial and sporadic schizophrenia and
their first degree relatives.
METHODSA weighted Waldrop assessment was carried
out on 214 subjects in five groups: schizophrenic patients from
multiply affected families; first degree relatives of these familial
schizophrenic patients; sporadic schizophrenic patients; first degree
relatives of these sporadic schizophrenic patients, and normal
controls. Broad and narrow criteria for abnormality were defined based
on the distribution of minor physical anomalies in the control group.
RESULTS(1) The total schizophrenic group did not
have a significant increase in minor physical anomalies using a narrow
criterion of abnormality, but did when a broader criterion was used.
(2) A significant increase in the proportion of subjects with an
abnormally high number of minor physical abnormalities was shown in the
group of sporadic schizophrenic patients (uncorrected p<0.01).
Separate analyses for males and females showed a significant increase
in the male sporadic group (uncorrected p<0.05), and a smaller
non-significant increase in the female sporadic group. Neither the
familial schizophrenic group nor either group of first degree relatives
showed any significant increases in the proportion of patients with
high abnormality scores.
CONCLUSIONThis work supports prenatal
developmental abnormality as a mechanism for sporadic, but not
familial, schizophrenia.
© 1998 by Journal of Neurology, Neurosurgery, and Psychiatry
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